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The neuron-specific deletion of SOCS3 increases leptin sensitivity through STAT3 activation, indicating that SOCS3 is an important negative feedback regulator of leptin signaling [99, 100]
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The disease is marked by fat droplets piling up in liver cells, chronic inflammation and scar tissue in the liver
doi: 10.1038/emm.2015.122
In the specific context of triple-agonism, it acts as a powerful driver of thermogenesis and fat oxidation
